Decreased gene expression of LC3 in peripheral leucocytes of patients with coronary artery disease

Wu, Guanghua; Wei, Guanghe; Huang, Jian; Pang, Shuchao; Liu, Lixin; Yan, Bo

doi:10.1111/j.1365-2362.2011.02486.x

Cited by 18 publications

(14 citation statements)

References 37 publications

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“…Autophagy markers were assessed in CD4 lymphocytes of males subjected to different exercise regimens or sedentary controls after 5 weeks of training; they found that exercise conditioning (especially high intensity interval training) triggers autophagy and suppresses apoptosis in lymphocytes when the subjects undergo a hypoxic exercise challenge 94 . The authors did not go so far as to suggest that the autophagic response in lymphocytes might reliably report on autophagy in other organs, but two studies by another group found a significant reduction in autophagy markers (by western blotting) in leukocytes of patients with coronary artery disease 95 or acute myocardial infarction 96 compared to healthy controls. However, none of these studies correlated autophagy markers in lymphocytes with those in heart tissue, so it remains to be seen whether peripheral blood cells represent a reliable reflection of autophagic activity in the heart.…”

Section: Methods To Measure Autophagy and Mitophagymentioning

confidence: 99%

Untangling Autophagy Measurements

Gottlieb

Andres

Sin

et al. 2015

Circulation Research

134

105

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Autophagy is an important physiological process in the heart, and alterations in autophagic activity can exacerbate or mitigate injury during various pathological processes. Methods to assess autophagy have changed rapidly as the field of research has expanded. As with any new field, methods and standards for data analysis and interpretation evolve as investigators acquire experience and insight. The purpose of this review is to summarize current methods to measure autophagy, selective mitochondrial autophagy (mitophagy), and autophagic flux. We will examine several published studies where confusion arose in in data interpretation, in order to illustrate the challenges. Finally we will discuss methods to assess autophagy in vivo and in patients.

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Section: Methods To Measure Autophagy and Mitophagymentioning

confidence: 99%

Untangling Autophagy Measurements

Gottlieb

Andres

Sin

et al. 2015

Circulation Research

134

105

View full text Add to dashboard Cite

show abstract

“…Lower levels of LC3-II (measured by Western blot) were observed in peripheral blood leukocytes in patients with coronary artery disease compared to age and sex-matched healthy controls 24 of peripheral blood lymphocytes with intracellular staining of membrane-associated LC3 25 . A number of commercial kits for this purpose are now available.…”

Section: Clinically Feasible Approaches To Monitoring Autophagymentioning

confidence: 94%

Measuring Autophagy in Vivo

Gottlieb

2013

Autophagy in Health and Disease

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“…We have previously reported altered LC3 gene expression levels in CAD and AMI patients [21]. Several genetic variants have been identified in the ATG7 and LC3 gene in AMI patients [22,23].…”

Section: Introductionmentioning

confidence: 92%

Functional Genetic Variant in ATG5 Gene Promoter in Acute Myocardial Infarction

Zhang

et al. 2020

Cardiology Research and Practice

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Coronary artery disease (CAD) including acute myocardial infarction (AMI) is an inflammatory and metabolic disease mainly caused by atherosclerosis. Dysfunctional autophagy has been associated with abnormal lipid metabolism and inflammation. In previous studies, we have reported altered autophagic activity in AMI patients. As autophagy-related protein 5 (ATG5) is a core protein in autophagy, we speculated that altered ATG5 level may contribute to CAD and AMI development. In this study, the promoter of the ATG5 gene was genetically and functionally investigated in large groups of AMI patients (n = 378) and ethnic-matched healthy controls (n = 386). The results showed that a total of 15 genetic variants including 6 single-nucleotide polymorphisms (SNPs) in the ATG5 gene promoter were found in this study population. A novel deletion variant (g.106326168_70delTCT) and an SNP [g.106325757C > G (rs190825454)] were found in one 66-year-old male patient with non-ST-segment elevated AMI, but in none of controls. In cultured HEK-293 and H9c2 cells, the deletion variant significantly decreased the transcriptional activity of the ATG5 gene promoter (P<0.01). In contrast, the genetic variants either identified only in controls or found in both AMI patients and controls did not affect the transcriptional activity of the ATG5 gene promoter (P>0.05). Furthermore, an electrophoretic mobility shift assay showed that the deletion variant evidently affected the binding of a transcription factor. Therefore, the genetic variant identified in AMI may affect the activity of the ATG5 gene promoter and change the ATG5 level, contributing to AMI as a rare risk factor.

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Decreased gene expression of LC3 in peripheral leucocytes of patients with coronary artery disease

Abstract: LC3 gene expression in the peripheral leucocytes was significantly decreased in patients with CAD, indicating that autophagosome formation is decreased. These data suggest that autophagy in circulating leucocytes may be involved in the pathogenesis of atherosclerosis and CAD.

Cited by 18 publications

References 37 publications

Untangling Autophagy Measurements

Untangling Autophagy Measurements

Measuring Autophagy in Vivo

Functional Genetic Variant in ATG5 Gene Promoter in Acute Myocardial Infarction

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